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Solanezumab, Lilly's anti-amyloid MAb, may provide some clinical benefit in patients with mild AD, according to data presented yesterday by the AD Cooperative Study group. The independent group presented pooled data from Lilly's 2 phase 3 studies (EXPEDITION 1 and 2) at the ANA meeting in Boston.

Among the results (according to Lilly's press release and MedPage Today)*:

• In patients with mild AD from EXPEDITION 1, solanezumab slowed cognitive decline (via the ADAS-cog11) by a statistically significant 42% (P = .008). However, the absolute difference between solanezumab- and placebo-treated patients was not provided, nor was the rate of decline of placebo-treated patients provided in the press release. (There was no treatment-related difference in ADCS-ADL scores.)

• In patients with mild AD from EXPEDITION 2, solanezumab slowed cognitive decline (via the ADAS-cog14**) by 20%; however, this difference was not statistically significant (P = .008). (There was a statistical trend toward a treatment-related difference in the ADCS-ADL scores [P = .076].)

• In patients with mild AD from EXPEDITION 1 and 2 (pooled data), solanezumab slowed cognitive decline (via the ADAS-cog14) by a statistically significant 34% (P = .001). (And there was a statistical trend toward a treatment-related difference in the ADCS-ADL scores [P = .057].) However, according to MedPage Today, the absolute score difference on the ADAS-cog14 was only 1.3 points per year.
  

The possible clinical effects of solanezumab did not appear to be dependent on APOE ε4 genetic status. Also curious was the outcome that solanezumab affected only some AD biomarkers in these post-hoc study populations. (The biomarker data will apparently be presented at the CTAD meeting in Monte Carlo later this month.)

Angina (?) was statistically significantly more common in solanezumab-treated patients (1.1% vs 0.2% with placebo). Vasogenic edema (ie, ARIA-E) occurred in 11 solanezumab-treated patients (~1%) and 5 placebo-treated patients (no statistical difference).

A more thorough assessment of these data is needed, specifically in peer-reviewed form, before certain assumptions (or hopes) about solanezumab can be concluded. It'd be really nice to know the cognitive decline of the placebo-treated groups. What raised hopes about bapineuzumab, Pfizer/JNJ's now-defunct anti-amyloid MAb, was the statistical difference between actively treated and placebo-treated groups in the phase 2 studies. However, the difference may have been artificial, because the placebo-treated patients declined at a more rapid rate than might be expected in AD.

Regardless of any reservations about solanezumab, Lilly's share price shot up about 8% (from ~$48 to ~$52) on the promising news.

ADAS-cog = Alzheimer Disease Assessment Scale-cognitive subscale; ADCS-ADL = Alzheimer Disease Cooperative Study-activities of daily living; ANA = American Neurological Association; APOE ε4 = apolipoprotein E, ε4 allele; ARIA-E = amyloid-related imaging abnormalities-edema; CTAD = Clinical Trials on Alzheimer Disease; EXPEDITION = Effect of LY2062430, an Anti-Amyloid Beta Monoclonal Antibody, on the Progression of Alzheimer's Disease as Compared With Placebo; MAb = monoclonal antibody.

* Unfortunately I can't find the actual abstract (or any filmed presentation) at the ANA meeting website.
** Lilly changed the prespecified primary outcome from ADAS-cog11 to ADAS-cog14.

The unequivocally negative clinical results of the phase 3 studies of bapineuzumab do little to promote or detract from the idea that accumulating amyloid in the brain is the instigator of Alzheimer disease. For continued supporters of the amyloid hypothesis, including Dr. Reisa Sperling, who presented the phase 3 results for APOE ε4 carriers at the recent EFNS meeting in Stockholm, the positive biomarker results (stabilization of brain amyloid* and reduction of CSF p-tau levels) suggest that we're either intervening too late in the condition or that we need to reduce the amyloid burden more significantly to see clinically meaningful benefits with anti-amyloid compounds.


In the phase 3 study of APOE ε4 carriers (who generally have a higher amyloid burden than noncarriers), ARIA-E was significantly more likely with bapineuzumab (0.5 mg/kg) than with placebo (15% [n = 103] vs 0.2% [n = 1]); although only a small minority of affected patients (n = 16) were symptomatic (eg, headache, confusion). Among serious adverse events, the imbalance between bapineuzumab- and placebo-treated patients was driven by the incidence of ARIA-E (2.1% vs 0).

In the phase 3 study the APOE ε4 noncarriers, the results of which were presented by Dr. Stephen Salloway, the biomarker effects were less robust than those in the carrier study; although there appeared to be a possible dose-related effect of bapineuzumab (1.0 vs 0.5 mg/kg) on these outcomes (ie, brain amyloid and p-tau). The incidence of ARIA-E was not as high in this study (9.4% with the 1.0-mg/kg dose vs 0.2% with placebo), probably because the amyloid burden was not as high in the enrollees (my conjecture, not Salloway's). Notably 36% of enrollees did not meet the cutoff value for amyloid positivity in the brain, suggesting that PET imaging in noncarriers is much less sensitive for supporting the diagnosis of AD (also my conjecture). Other concerning safety data indicate that intracranial hemorrhage and seizure are more likely with higher doses of bapineuzumab.

The webcasts of both presentations at the EFNS can be found here and here. However, the all-important follow-up Q&A session was not recorded (or made available for online presentation).

ADAS-cog = Alzheimer's Disease Assessment Scale, cognitive subscale; ARIA-E = amyloid-related imaging abnormalities, edema; CSF = cerebrospinal fluid; MAb = monoclonal antibody; p-tau = phosphorylated tau.
* Via PiB PET [Pittsburgh compound B with positron emission tomography].

N.B.--According to MarketWatch (and other sources), "Pfizer and J&J continue to study a subcutaneous formulation of bapineuzumab, and it's possible that formulation could be tested in patients with early stages of Alzheimer's." Given the phase 3 results, it's unlikely that a SQ formulation is going to be more efficacious (while possibly being safer) than an IV version of bapineuzumab. However, the primary intent here may be to prove safety, while reserving the possibility of efficacy for early-intervention studies. But the future remains dim for bapineuzumab in whatever form, IMHO.

Lilly effectively made a small cup of lemonade out of 2 big lemons on Friday, when the company released its expected, negative phase 3 results of solanezumab in mild-moderate Alzheimer disease. The anti-amyloid MAb, when compared with placebo, did not significantly alter the cognitive or functional primary outcomes* in either study of approximately 1000 patients each.

But—but, Lilly says—when data were pooled from both studies, the firm was able to squeeze out a "statistically significant slowing of cognitive decline" in the overall population and in patients with mild AD specifically. Although Lilly didn't say what the specific secondary cognitive outcome was (there are only a few prespecified options**) and what the actual difference was. It seems unlikely that the difference would be related to the crudest, secondary cognitive measure, the MMSE score.

The next best option, unless Lilly added another secondary cognitive outcome after its interim assessment of data (which may be the case), is a statistical difference in the Clinical Dementia Rating—Sum of Boxes (CDR-SB). Although the CDR-SB is more of a global functioning score, assessing memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. When calculating the CDR-SB, each of the 6 domains is rated (based on information from patient and caregiver interviews) on a 4- or 5-point scale (from 0 or 0.5 to 3). The domain scores are then added for the sum-of-boxes score (which ranges from 0 to 18). I can only surmise that Lilly is implying some kind of statistical difference on the basis of this more qualitative and less precise score between the pooled placebo- and solanezumab-treated groups, which I don't find to be a particularly promising outcome in the face of the other negative results. To me, this seems like more smoke from a phase 3 crash and burn than anything. But the result may provide momentum to those who want to test the drug in earlier phases of AD, specifically mild cognitive impairment (MCI). The forward-looking statements from Lilly execs:

• John Lechleiter,CEO: "We intend to discuss these data with regulatory authorities to gain their insights on potential next steps."
• Jan Lundberg, President of Lilly Research Laboratories: "We believe the pooled data support the amyloid hypothesis, as these are the first Phase 3 data with an anti-beta amyloid agent that appear to show a slowing of cognitive decline."

That last statement appears to be a bold one.

As far as adverse events from the phase 3 trials are concerned, the most common with solanezumab treatment were lethargy, rash, malaise, and angina (?). Importantly no vasogenic brain edema was reported, as in studies of another (and now defunct) anti-amyloid MAb, bapineuzumab. It's a curious finding, or lack of a finding, if the side effect is believed to indicate the immune-mediated mobilization of amyloid out of the brain through vascular channels. Like in the bapineuzumab studies, what will be interesting to learn is whether Lilly's compound removed brain amyloid (via PET or other biomarkers), particularly in those patients who ostensibly experienced some clinical benefit with treatment.

The phase 3 results will be independently assessed by the AD Cooperative Study, and the group will present the results at the upcoming ANA meeting in early October, according to Lilly's press release. Just how Lilly manipulated the phase 3 studies to achieve the positive secondary outcome, what the secondary measure was, what the quantitative difference was, and the nature of the placebo-treated group (eg, the group's level of cognitive decline) will be vital to know.

MMSE = Mini-Mental State Examination; PET = positron emission tomography.

* Change from baseline to endpoint in Alzheimer's Disease Assessment Scale—Cognitive subscore (ADAS-Cog11) at 80 weeks; and change from baseline to endpoint in Alzheimer's Disease Cooperative Study—Activities of Daily Living Inventory (ADCS-ADL) at 80 weeks.
** The secondary outcomes measures for both EXPEDITION trials were the Clinical Dementia Rating—Sum of Boxes (CDR-SB), the Neuropsychiatric Inventory (NPI), the MMSE, the Resource Utilization in Dementia—Lite (RUD-Lite), 2 quality-of-life measures, a volumetric MRI measure, and 2 biomarker measures.

Aaaand, it's over. Yesterday (after the bell), Pfizer and Janssen announced the discontinuation of their development program for IV bapineuzumab, the anti-amyloid MAb for Alzheimer disease on which many high and low expectations were placed. It appears that the low expectations (expressed, in particular, at this blog) were accurate. The phase 3 efficacy results for the MAb in noncarriers of the AD risk allele APOE ε4 were negative, in addition to the recently announced negative phase 3 results for APOE ε4 carriers. Consequently the whole program has been scrapped, including any extension studies and 2 other ongoing phase 3 trials.*

Pfizer says that the results of the negative phase 3 studies will be presented at the upcoming EFNS meeting in Stockholm. What to look for: the degree to which bapineuzumab cleared brain amyloid (via PET imaging) and safety issues, specifically the incidence of ARIA. According to the press release, the most commonly observed serious AEs with bapineuzumab (ie, more common than with placebo and at a frequency of at least 1%) included ARIA-E (eg, vasogenic edema). Pfizer has told inquiring news sources that there are no plans to study bapineuzumab in earlier phases of AD (ie, MCI), but the option (if it's ever picked up) rests on the safety of the MAb in the completed phase 3 trials in AD.

As far as I can tell, Pfizer/Janssen's only other viable joint candidate for AD treatment is an anti-amyloid vaccine, ACC-001, which is in phase 2 development. Given that there's now very slim hope for the clinical success of an anti-amyloid treatment in established AD (despite the fact that bapineuzumab appeared to remove amyloid from the brain), companies currently invested in the therapeutic strategy (for instance, Roche and GSK, along with Pfizer and Janssen) must seriously reassess their commitments. Roche's crenezumab was recently selected for testing in a Colombian family with a deterministic gene for AD, so the study population here appears to be more promising. GSK's candidate drug is (I believe) in phase 1 development. The phase 3 results for Lilly's solanezumab in AD are, of course, expected imminently, and the chance of success, although very low, is not zero. Lilly's MAb may target a more toxic version of amyloid (ie, soluble amyloid) than bapineuzumab (which was believed to be more specific for sequestered, insoluble amyloid in neuritic plaques). But that explanation may be more marketing than science.

* Although an imaging study with SQ bapineuzumab continues.

AEs = adverse events; ARIA = amyloid-related imaging abnormalities; MAb = monoclonal antibody; MCI = mild cognitive impairment; PET = positron emission tomography.

In a development that isn't terribly surprising, Pfizer released disappointing data yesterday evening from its (and Janssen's) phase 3 study of the anti-amyloid MAb bapineuzumab in patients with mild-moderate Alzheimer disease. This study, in which enrollees carry 1 or 2 APOE ε4 alleles (a risk factor for AD and a higher burden of brain amyloid), did not meet its co-primary clinical endpoints: a change in cognitive and global functions. Details of this trial, and those of a companion trial of bapineuzumab in non-APOE ε4 carriers, will be presented in early September at the EFNS meeting in Stockholm.

The enrollees (APOE ε4 positive) who received bapineuzumab in the negative phase 3 study will not receive the treatment in an extension of the trial, but they will undergo follow-up, Pfizer says. What will be interesting to learn more about from this study (labeled 302) is 1) whether there was definite PET evidence of amyloid clearing in the bapineuzumab-treated patients; and 2) whether some portion of these patients developed asymptomatic or symptomatic ARIA (eg, vasogenic edema or microhemorrhages)—findings which have been linked to the immune-mediated clearance of amyloid from the brain.

Pfizer also reminds us that 2 other phase 3 studies of bapineuzumab are underway (see the table here for a list of registered bapineuzumab studies), the results of which are expected in 2013 and 2014. One of these studies is in APOE ε4 carriers. Depending on the imminent outcome of the phase 3 study of the MAb in non-APOE ε4 carriers, perhaps Pfizer and Janssen will make a decision about the developmental fate of bapineuzumab. Maybe they will forgo further investigation of the MAb in frank AD and focus on earlier stages of dementia—namely, MCI. A big part of that decision will rest on the relative safety and tolerability of bapineuzumab in the most-advanced phase 3 trials of AD.

ARIA = amyloid-related imaging abnormalities; MAb = monoclonal antibody; MCI = mild cognitive impairment; PET = positron emission tomography.

IV immunoglobulin (specifically Baxter's Gammagard) may halt the progression of Alzheimer's disease, according to a very small extension study of the twice-weekly drug. Phase 2 results, presented at the ongoing AAIC in Vancouver, indicated that 4 patients who received the standard dosage (0.4 mg/kg) every 2 weeks for the full 3 years of the extension study demonstrated no decline in accepted clinical measures of cognition, daily or global functioning, behavior, or quality of life. That's a remarkable finding, even with the limited subject number, in a disease that is known to progress inexorably. Unless the diagnosis of AD was made in error in these 4 patients, or there was some confounding variable in their assessment (like the influence of unblinded treatment), it seems that these results should be valid and potentially reproducible on a larger scale.

Also according to the AAIC press release: Among the 16 of 24 patients who elected to participate in the phase 2 extension study of IV Ig, 11 patients who received the treatment for 3 years (with 7 of these patients presumably receiving a dosage below 0.4 mg/kg) "had favorable outcomes in terms of their thinking abilities, behavior and daily function." Among the 5 participants who initially received placebo treatment, switching to IV Ig in the extension phase was associated with a less rapid decline in AD-related symptoms. The drug, however, was not without its safety issues, according to coverage by MedPage Today. At least one patient experienced a stroke, possibly as a result of increased blood viscosity associated with IV Ig therapy.

Notably there are at least 2 phase 3 studies evaluating Baxter's Gammagard in mild-moderate AD, one of which is actively recruiting subjects. Results of an ongoing 18-month trial (N = 390) are expected in February of next year. One thing that would be very interesting, if not crucial, to know is whether the stabilization of clinical AD with IV Ig (if it is confirmed) is associated with the removal of brain amyloid. Unfortunately it is not stipulated in the phase 3 trial description that subjects are undergoing PET imaging for amyloid.

Gammagard is FDA approved for a number of immune-mediated or immunodeficiency diseases, and it is used off label for several neurologic conditions, including inflammatory neuropathies. Consequently the uptake of IV Ig by neurologists for the treatment of AD, if it is determined to be reliably effective, will be relatively swift. Lead investigator of the phase 2 study, Norman Relkin, cautioned against the current use of IV Ig for AD, given that supplies of the blood-derived product are limited, and that the lives of some patients with FDA-approved indications are dependent on available treatment. "[W]e don't want to bankrupt the available supplies," he advised MedPage Today.

AAIC = Alzheimer's Association International Conference; IV Ig = intravenous immunoglobulin.

A first-of-its-kind, longitudinal study of PET imaging for amyloid suggests that the brain scan may help predict further cognitive decline in patients with mild cognitive impairment (MCI); although brain imaging for amyloid continues to have its significant limitations. In this 18-month study (N = 151), with Avid/Lilly's newly approved Amyvid radioactive tracer, the rate of conversion from MCI* to Alzheimer disease** approached 30% in patients with positive amyloid scans and was only about 10% in patients with negative scans; although the difference in this relatively small study did not reach statistical significance (P = .0996). In addition, evidence of cognitive decline was statistically significantly more likely in people with MCI or normal cognition who demonstrated amyloid on PET images.

However, three very important caveats to this study are in order:

1. Positive PET imaging for amyloid remains a relatively insensitive and nonspecific marker for cognitive dysfunction or even frank, AD-consistent dementia. Only about two-thirds of patients with AD demonstrated amyloid on PET images, and 14% of subjects with normal cognition (age, ≥50 years; MMSE score, 29-30) showed tracer-tagged amyloid. Moreover, although amyloid positivity in patients with AD was more likely to be associated with a higher ADAS-cog score at baseline, the finding was not useful for predicting a more rapid rate of cognitive decline in this subgroup.
   
   
2. Nearly as many patients with MCI converted to normal cognition (n = 7/46) as those who converted to AD (n = 8/46) during follow-up. These data suggest that the clinical diagnosis of MCI in this study was fairly loose and probably erroneous in some cases (if you believe that MCI is a clinical prodrome of inevitable AD, as many do). However, the baseline rate of amyloid positivity in the MCI subgroup was 37%, and patients who did not demonstrate brain amyloid were more likely to convert to normal cognition (although the rate of conversion to normal cognition in amyloid-positive patients [6%] and that in amyloid-negative patients [21%] was not statistically significantly different).
   
   
3. The accurate reading of these scans remains problematic. The agreement between 3 blinded readers in this study was only 74%. The FDA's approval of Amyvid has been criticized (for instance, by Public Citizen) for the lack of agreement among scan readers; although the agency has attempted to mitigate this problem with a mandatory reader-training program.
   

In a related editorial, Drs. Ansgar Furst and Goeffrey Kercher of Stanford generally agree that Amyvid "may play a clinically useful role in predicting the risk of cognitive decline among patients with MCI." But they also advise,

In patients who have already crossed the threshold to dementia, the lack of a close association between [Amyvid] and cognitive/functional status is not surprising since 1) A
burden appears to remain fairly constant once amyloid positivity is reached, and 2) amyloid burden is no longer the driving force for disease progression once the clinical diagnosis of AD has been reached. Its use in such patients will therefore be restricted to differential diagnosis. For cognitively normal individuals, there is not yet a role for amyloid imaging in screening for AD risk.

Notably a 36-month extension of this study is underway.

ADAS-cog = Alzheimer's Disease Assessment Scale, cognitive subscale.

* Average MMSE score, 27-28.
** Average MMSE score, 21-22.

Image of amyloid-positive PET scan in patient with MCI who converted to AD during the study (Doraiswamy et al. Neurology. 2012;Jul 12. [Epub before print]).

The process of Alzheimer disease begins years, if not decades, before the onset of clinical dementia, according to a newly published study in the New England Journal of Medicine. In the Dominantly Inherited Alzheimer Network, or DIAN, trial, patients who are genetically destined to acquire AD (a small minority of AD cases) showed physiologic signs of the underlying disease process well before the onset of any cognitive dysfunction.

According to the prospective, longitudinal study, which included 88 people who carry a deterministic gene for AD and 40 controls:

• CSF levels of amyloid beta (Aβ) 42, an indirect marker of Aβ deposition in the brain, began declining 25 years before the expected onset of clinical dementia.*
• Evidence of Aβ on PET scans, increasing levels of CSF tau, and hippocampal atrophy (via MRI) were seen 15 years before the expected expected onset of clinical dementia.
• Ten years before expected overt dementia, evidence of cerebral hypometabolism (per FDG-PET) and mild clinical symptoms in the form of episodic memory loss were observed.
  
• Dementia, on the basis of diagnostic criteria, was seen 3 years before its expected onset (suggesting that the recognition of dementia in practice—outside of a longitudinal study—is typically delayed by at least a few years).

While the DIAN study authors caution that confirmation of their data is needed and that these results shouldn't necessarily be applied to the subclinical progression of sporadic AD (the overwhelmingly most common form of AD), a generalization of their findings does not seem unreasonable and is, moreover, highly likely.

If valid and generalizable, the DIAN biomarker data suggest that abnormalities in the CNS production and/or deposition of Aβ42 are the very earliest signs of AD (notably years before evidence of tau abnormalities). Consequently the use of anti-Aβ42 compounds, despite their relative disappointment in established AD (on the basis of phase 2 studies), remains at least theoretically viable in nascent disease—like in MCI. But even so, effective interventions in AD may need to be applied long before there is any clinical hint of illness.

CNS = central nervous system; CSF = cerebrospinal fluid; FDG = fluorodeoxyglucose; MCI = mild cognitive impairment; MRI = magnetic resonance imaging; PET = positron emission tomography.

* Estimated on the basis of the age of onset of clinical dementia in the affected parent.

The highly anticipated phase 3 results for two anti-amyloid MAbs in Alzheimer disease will be presented in October at the meeting of the "Clinical Trials on Alzheimer's Disease" (CTAD) in Monte Carlo, Monaco. Whether the results of the clinical trials will be presented at earlier meetings or even by press releases is unknown (to me). Of the handful of major meetings where AD clinical results might be presented—the AAIC in mid-July, the EFNS in early September, the ICADD in mid-September, and the ANA in early October—none has listed (as yet) the scheduled presentation of phase 3 results for Pfizer/Janssen's bapineuzumab or Lilly's solanezumab.

According to the CTAD program (found here), the phase 3 results for bapineuzumab will be presented at a 1-hour symposium on Monday, October 29th, at 11:15 am. Speakers will be Reisa Sperling (of Brigham and Women's in Boston), Stephen Salloway (of Brown University in Providence, Rhode Island), and Nick Fox (of University College, London). The symposium moderator will be Philip Scheltens (of the VU Medical Center in Amsterdam).

The solanezumab trial results will be presented by Eric Siemers, Senior Medical Director for Lilly's AD Team, on Tuesday, October 30th, from 11 am to noon. No other speakers or moderators are listed for this symposium in the CTAD program.

AAIC = Alzheimer's Association International Conference; ANA = American Neurological Association; EFNS = European Federation of Neurological Societies; ICADD = International Conference on Alzheimer's Drug Discovery; MAb = monoclonal antibody.

06/21/12 addendum: The phase 3 trial results for solanezumab and bapineuzumab will also be incorporated into an afternoon symposium at the ANA meeting in early October. In a 2-hour presentation entitled, "Results of Immune-Based Trials in Neurological Disorders," scheduled for Monday, October 8th at 1:15 pm, several speakers and panelists (listed here) will discuss...

"...the pathogenetic context for immunotherapy, a Phase III Study of Solaneuzumab [sic] for Alzheimer's disease, Phase III study results of Bapineuzumab results [sic], a Phase II Study of Immunotherapy in Multiple Sclerosis, and an immunotherapy approach to pain..."

Last Thursday, the phase 2 results of solanezumab, Lilly's anti-amyloid MAb, were published online in Alzheimer's & Dementia (the official journal of the Alzheimer's Association). Notably the phase 2 development of solanezumab has been severely truncated at 12 weeks, ostensibly to move the MAb quickly into phase 3 trials in an effort to catch up with the late-phase development of another anti-amyloid MAb competitor, Pfizer/Janssen's bapineuzumab.

Not surprisingly there was no reported evidence of clinical improvement with weekly infusions of solanezumab in this abbreviated and small placebo-controlled study (N = 52).* But the MAb appeared to be reasonably well tolerated and safe, outcomes of which are the crux of phase 2 assessment. Importantly there was no evidence of vasogenic brain edema on MR images or meningoencephalitis, findings that have plagued the late-phase development of bapineuzumab and an anti-amyloid vaccine (AN1792), respectively. The MAb also appeared to increase the CSF level of amyloid beta(1-42) in a dose-dependent fashion, a result suggesting (in the authors' words) that "this antibody may shift [amyloid beta] equilibria sufficiently to mobilize [amyloid beta]1-42 from amyloid plaques."

A substudy of 24 patients, incorporating baseline and 12-week SPECT imaging for amyloid,** will be reported separately, the authors note. Results of the imaging substudy should support the removal of brain amyloid with the MAb. Phase 3 results for both solanezumab and bapineuzumab are expected imminently—meaning sometime this summer or, at least, in the early autumn.

CSF = cerebrospinal fluid; MAb = monoclonal antibody; SPECT = single-photon emission computed tomography.
* 42 patients received solanezumab, and 10 received placebo.
** Interesting that they're not using Lilly's just-approved PET amyloid tracer, florbetapir (Amyvid).